Formation of cleft palates in mouse embryos may be induced in response to the administration of a glucocorticoid (e.g., cortisol or triamcinolone) at day 12.5 of gestation. The biochemical mechanism underlying the formation of such a cleft palate is at present unknown. It is known, however, that glucocorticoid administration to pregnant mice at specified times leads to a halt in processes necessary for fusion of the palate in the embryos. Hence, some of the questions being asked under this research program include: "Are there changes in gene expression resulting from the administration of a teratogen to a developing system? Can the formation of a cleft palate be a consequence of aberration in genetic expression?" Therefore, my continuing objective is to study the mechanism of action of glucocorticoids in developing palates at the nuclear level, and to test the hypothesis whether glucocorticoid incorporation into nuclei results in a specific inhibition in the synthesis of essential messenger RNA's. Thus, the binding of triamcinolone to chromatin may be reflected in the base sequences of mRNA's transcribed in vivo in cleft palates when compared to mRNA's found in normal developing palates. Other studies are also proposed to obtain evidence to show whether triamcinolone remains associated to chromatin once it becomes exposed to it in vivo, or if the glucocorticoid is dissociated in time from chromatin, leaving the affected chromatin abnormally expressed. The methods proposed include studies on the binding of triamcinolone to chromatin and to nonhistone chromosomal proteins. Hybridization of RNA to DNA of unique sequences will also be done in order to obtain information on possible occurrence of modification in genetic expression during development of both normal and cleft palates (in response to triamcinolone).